ReviewOxidative medicine and cellular longevity2017
ROS: Crucial Intermediators in the Pathogenesis of Intervertebral Disc Degeneration.
Review in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
243 citing papers in PubMed, 1 synthesis or guideline pooled it, 378 citations in OpenAlex.
- Extracellular Vesicles as an Emerging Treatment Option for Intervertebral Disc Degeneration: Therapeutic Potential, Translational Pathways, and Regulatory Considerations.Advanced healthcare materials · 2022Pooled it
- Comparative effect of transforaminal injection of Magnesium sulphate versus Ozone on oxidative stress biomarkers in lumbar disc related radicular pain.BMC anesthesiology · 2022Trial
- Biomaterials for intervertebral disc regeneration: Niche reprogramming, precision therapeutics, and structural reconstruction.Bioactive materials · 2027Review
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 2026Review
- Intradiscal Delivery of Notoginsenoside R1-Loaded PLGA Nanoparticles Attenuates Intervertebral Disc Degeneration in Rats.Journal of cellular and molecular medicine · 2026Article
- Ergothioneine-Derived Carbon Dot Nanozymes Alleviate the Oxidative Stress Microenvironment to Delay Intervertebral Disc Degeneration.Antioxidants (Basel, Switzerland) · 2026Article
- Thrombospondin-4 Regulates Lipopolysaccharide-Induced Apoptosis and Inflammation in Nucleus Pulposus Cells via the Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway.Immunity, inflammation and disease · 2026Article
- Mitigating nucleus pulposus cell senescence in intervertebral disk degeneration: the role of nodakenin in SIRT6 and PINK1/Parkin-associated mitophagy signaling.Cellular & molecular biology letters · 2026Article
- Application of cerium dioxide nanoparticles in the treatment of intervertebral disc degeneration induced by oxidative stress.Journal of translational medicine · 2026Article
- Current Perspective on Orthobiology Applications for the Treatment of Intervertebral Disc Degeneration (IDD)-A Narrative Review.Medicina (Kaunas, Lithuania) · 2026Review
- Adapt, Mitigate, and Target: The Role of Oxidative Stress in Intervertebral Disc Homeostasis and Disc Degeneration.Neurospine · 2026Review
- ROS-Responsive Wedelolactone Hydrogel Promotes Intervertebral Disc Repair by Disrupting the NF-κB-LCN2 Inflammatory Feedback Loop.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A New Direction for Delaying Intervertebral Disc Degeneration: Resveratrol Inhibits Ferroptosis in Nucleus Pulposus Cells.Cell biochemistry and biophysics · 2026Article
- METTL3-mediated GLUD1 m6A Modification Promotes Hydrogen Peroxide-induced Mitochondrial Dysfunction in Human Nucleus Pulposus Cells Via the Glutamate/α-KG Metabolic Axis.Journal of musculoskeletal & neuronal interactions · 2026Article
- Immunometabolism: A Novel Therapeutic Target and Its Pharmacological Modulation for Intervertebral Disc Degeneration.International journal of molecular sciences · 2026Review
- Etiology, diagnosis and treatment of lumbar disc degeneration: a focus on the mechanism of action of Piezo1 and research perspectives.Frontiers in cell and developmental biology · 2026Review
- Region-dependent expression and function of integrin α5β1 in protecting against disc degenerationFrontiers in bioengineering and biotechnology · 2026Article
- Iron, lipid peroxidation and discogenic pain: a redox framework for ferroptosis in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2026Review
- Cellular and molecular mechanisms of diabetes-mediated disc degeneration.Frontiers in endocrinology · 2026Review
- Metabolic reprogramming in intervertebral disc degeneration: mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
183 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive reactive oxygen species (ROS) generation in degenerative intervertebral disc (IVD) indicates the contribution of oxidative stress to IVD degeneration (IDD), giving a novel insight into the pathogenesis of IDD. ROS are crucial intermediators in the signaling network of disc cells. They regulate the matrix metabolism, proinflammatory phenotype, apoptosis, autophagy, and senescence of disc cells. Oxidative stress not only reinforces matrix degradation and inflammation, but also promotes the decrease in the number of viable and functional cells in the microenvironment of IVDs. Moreover, ROS modify matrix proteins in IVDs to cause oxidative damage of disc extracellular matrix, impairing the mechanical function of IVDs. Consequently, the progression of IDD is accelerated. Therefore, a therapeutic strategy targeting oxidative stress would provide a novel perspective for IDD treatment. Various antioxidants have been proposed as effective drugs for IDD treatment. Antioxidant supplementation suppresses ROS production in disc cells to promote the matrix synthesis of disc cells and to prevent disc cells from death and senescence in vitro. However, there is not enough in vivo evidence to support the efficiency of antioxidant supplementation to retard the process of IDD. Further investigations based on in vivo and clinical studies will be required to develop effective antioxidative therapies for IDD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.